Vitexin Ameliorates HG-Induced Injury in Retinal ARPE-19 Cells by Targeting CASP3.

Area of Science:

• Ophthalmology
• Pharmacology
• Cell Biology

Background:

• Diabetic retinopathy (DR) is a leading cause of vision loss due to diabetes mellitus.
• Vitexin shows promise in treating inflammatory eye conditions and neuronal damage.
• The efficacy and mechanism of vitexin in DR treatment are currently unknown.

Purpose of the Study:

• To investigate the protective effects of vitexin on retinal cells against high glucose (HG)-induced damage.
• To elucidate the underlying mechanism of vitexin's action in the context of diabetic retinopathy.
• To explore vitexin's potential as a therapeutic agent for early DR.

Main Methods:

• Cell viability was assessed using the Cell Counting Kit-8 (CCK-8) assay.
• Oxidative stress, apoptosis, and inflammation were evaluated using flow cytometry, thiobarbituric acid assay, commercial kits, and western blot analysis.
• Bioinformatics analysis, including Swiss Target Prediction, CTD, Gene Cards, and molecular docking, was employed to identify the molecular target.

Main Results:

• Vitexin mitigated oxidative stress by reducing malondialdehyde (MDA) and reactive oxygen species (ROS) and enhancing superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity.
• Vitexin attenuated inflammatory responses by suppressing tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) while promoting interleukin-10 (IL-10), thereby reducing apoptosis.
• Molecular docking and gene screening identified caspase-3 (CASP3) as a key interaction target; overexpressing CASP3 diminished vitexin's protective effects.

Conclusions:

• Vitexin exerts cytoprotective effects on ARPE-19 cells against high glucose-induced damage.
• The protective mechanism of vitexin in early DR is mediated through the caspase-3 (CASP3) pathway.
• Vitexin demonstrates potential as a therapeutic agent for managing diabetic retinopathy.